Distribution of actin filaments, non-muscle myosin, M-Ras, and extracellular signal-regulated kinase (ERK) in osteoclasts after calcitonin administration
Distribution of actin filaments, non-muscle myosin, M-Ras, and extracellular signal-regulated kinase (ERK) in osteoclasts after calcitonin administration
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DOI：
10.1679/aohc.68.143
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发表时间：
2005-06-01
影响因子：
--
通讯作者：
Yamamoto, T
中科院分区：
文献类型：
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作者：
Nakamura, H;Nagaoka, N;Yamamoto, T
用扫描电镜观察降钙素对大鼠胫骨破骨细胞内肌动蛋白丝分布的影响。荧光显微镜检查降钙素诱导的肌动蛋白丝，非肌肉肌球蛋白，M-Ras和细胞外信号调节激酶（ERK）的分布的变化，以澄清ERK在破骨细胞的细胞骨架中的作用。对照组破骨细胞的扫描电镜显示在外周区域有环状结构。标记的肌动蛋白丝和非肌肉肌球蛋白在外周区域被检测到，并表现出环状图案。在肌动蛋白环附近也检测到指示M-Ras和ERK的免疫反应性。降钙素治疗后，许多破骨细胞表现出收缩的外观，缺乏可辨别的肌动蛋白环。在降钙素处理的破骨细胞的边缘发现大量的收缩纤维。肌动蛋白丝和非肌肉肌球蛋白集中在降钙素处理的破骨细胞的细胞质中，并表现出丝状模式。标记的M-Ras和ERK也聚集在这些破骨细胞的中心区域。这些结果表明肌动蛋白-肌球蛋白相互作用在降钙素诱导的破骨细胞收缩中起着重要作用。ERK可能通过激活肌球蛋白轻链激酶在这种相互作用中发挥作用，如先前在平滑肌细胞中观察到的。
Scanning electron microscopy (SEM) was employed to study the effect of calcitonin on the distribution of actin filaments in osteoclasts obtained from rat tibiae. Fluorescent microscopy was also applied to examine calcitonin-induced changes in the distribution of actin filaments, non-muscle myosin, M-Ras, and extracellular signal-regulated kinase (ERK) to clarify the role of ERK in the cytoskeleton of osteoclasts. SEM of control osteoclasts revealed a ring-like structure in the peripheral region. Labeled actin filaments and non-muscle myosin were detected in the peripheral region and exhibited a ring-like pattern. Immunoreactivity indicating M-Ras and ERK was also detected in the vicinity of the actin ring. After calcitonin treatment, many osteoclasts exhibited a retracted appearance and lacked a discernible actin ring. Numerous retraction fibers were found at the edge of calcitonin-treated osteoclasts. Actin filaments and non-muscle myosin were concentrated in the cytoplasm of calcitonin-treated osteoclasts, and exhibited a filamentous pattern. Labeled M-Ras and ERK also accumulated in the central region of these osteoclasts. These findings suggest that actin-myosin interaction plays an essential role in the retraction of osteoclasts induced by calcitonin. ERK may play a role in this interaction by activating myosin light chain kinase, as previously observed in smooth muscle cells.